To the best of our knowledge, this is the first study reporting prevalence of NSSI defined by suggested DSM-5 criteria among adolescent in rural China. In comparison to finding from the similar samples of adolescents, Chinese rural adolescents seem to have a relative higher prevalence. The potential risk factors for NSSI include female, father's education, Han ethnicity, psychosocial factors and suicide behaviors. More evidence for further understanding of context of the occurrence, improving access to health care utilization, and identifying the role of psychosocial factors and family relationship, is needed for the prevention and management of NSSI.

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Circular RNAs (circRNA) are a new member of endogenously produced noncoding RNAs that have been characterized as key regulators of gene expression in a variety of malignances. However, the role of circRNA in oral squamous cell carcinoma (OSCC) remains largely unknown. In this study, we identified unique circRNA that regulate OSCC progression and metastasis and pave roads for future research in early diagnosis, prevention, and treatment of OSCC. Transcriptomic analyses identified a circRNA derived from IGHG locus (circIGHG) as significantly upregulated in OSCC and positively associated with poor prognosis of OSCC. circIGHG directly bound miR-142-5p and consequently elevated IGF2BP3 activity. Knockdown of circIGHG led to impaired expression of IGF2BP3 and attenuated aggressiveness of OSCC cells. Epithelial–mesenchymal transition was the main mechanism through which circIGHG/IGF2BP3 promotes metastasis of OSCC. Overall, these results demonstrate that circIGHG plays a pivotal role in OSCC development and metastasis and has potential to serve as a biomarker and therapeutic target for early-stage diagnosis and treatment of OSCC. Significance: These findings broaden our insights regarding regulation of OSCC progression by circular RNA and serve as a reference for future clinical research in OSCC diagnosis and treatment.

Background & Aims: Macrophages (Mu) represent a major component of tumor tissues and play an important role in both tumor progression and therapeutic response. Although tumor Mu are generally considered to be derived from circulating monocytes, emerging evidence indicates that tissue Mu pools can be maintained by self-renewal. We aimed to elucidate the contribution, phenotype, and regulatory mechanisms of proliferating Mu in human hepatocellular carcinoma (HCC). Methods: Flow cytometry analyses were performed to examine the presence and phenotype of proliferating Mu in fresh HCC tissues. Dual immunofluorescence staining was applied to analyze the prognostic value of proliferating Mu. The underlying regulatory mechanisms were examined using human monocytederived Mu. Results: Tumor-infiltrating Mu exhibited a significantly higher proliferative capacity than Mu in non-tumor tissues. A higher level of Mu proliferation was positively correlated with Mu density in the tumor and a poor prognosis in patients with HCC. Proliferating Mu were less differentiated (with increased CD206 expression) and were induced by the tumor cell-derived soluble small molecule, adenosine, but not proteins, lipids, or large peptides. Mechanistic studies demonstrated that autocrine granulocyte-macrophage colony-stimulating factor (GM-CSF) released by tumor-stimulated Mu could enhance A2A receptor expression on Mu and function synergistically with adenosine to elicit Mu proliferation in HCC. Conclusions: Local Mu proliferation is an important mechanism for Mu accumulation in HCC tissues. Tumor-derived adenosine functions synergistically with autocrine GM-CSF released from activated Mu, which promotes Mu proliferation. Thus, selective modulation of Mu accumulation at the source may provide a novel strategy for cancer therapy. Lay summary: Tumor-associated macrophages (TAMs) have been reported to play an essential role in both tumor progression and therapeutic response. A fundamental understanding of the mechanisms that regulate macrophage accumulation in tumors will undoubtedly lead to the development of strategies to target macrophages with high specificity and efficiency. The current study unveils a novel mechanism by which local proliferation is linked to macrophage accumulation in the tumor milieu, identifying potential targets for future immune-based anticancer therapies.

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